COMMON QUESTIONS AND ANSWERS IN THE MANAGEMENT OF HYPERTENSION Debbie L. Cohen, MD; Raymond R. Townsend, MD, Section Editors
The Salt Controversy and Hypertension
Article first published online: 13 FEB 2012
© 2012 Wiley Periodicals, Inc.
The Journal of Clinical Hypertension
Volume 14, Issue 4, pages 265–266, April 2012
How to Cite
Cohen, D. L. and Townsend, R. R. (2012), The Salt Controversy and Hypertension. The Journal of Clinical Hypertension, 14: 265–266. doi: 10.1111/j.1751-7176.2012.00594.x
- Issue published online: 28 MAR 2012
- Article first published online: 13 FEB 2012
Excess sodium intake is linked to higher blood pressure (BP), which, in turn, increases risk of stroke, coronary artery disease, heart failure and renal disease. However, defining “excess” sodium intake is controversial. Dietary Guidelines for Americans 2005 recommended that specific groups (persons with hypertension, all middle-aged and older adults, and all blacks [ie, 70% of the US adult population]) should limit sodium intake to 1500 mg/d.1 For other adults, the recommendation is <2300 mg/d.1 The Institute of Medicine supports these guidelines,2 the basis being that decreasing daily sodium consumption to 2300 mg/d (or less) would result in fewer cases of hypertension and cardiovascular (CV) death, thereby decreasing the costs associated with hypertension ($73.4 billion in 2009).
Using the National Health and Nutrition Examination Survey (NHANES) data for 2005 to 2006, the Centers of Disease Control and Prevention estimated average daily sodium intake and sources of sodium and calories by food category in US adults. They reported that only 5.5% of adults consumed <1500 mg of sodium per day and only 18.8% of adults consumed <2300 mg/d of sodium. Only 9.6% of adults adhered to the recommended sodium intake outlined above.3 About 10% of the sodium intake comes from discretionary sources (table salt and salt added while cooking), making sodium restriction difficult to accomplish.4
Recent studies now suggest that both low and high sodium intake are harmful and that dietary salt intake should be limited to around 4 g/d to 5 g/d (1 g of salt = 400 mg of sodium). A recent publication by O’Donnell and colleagues5 demonstrated the association between urinary sodium excretion and CV events may be J-shaped, based on data from the Ongoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomized Assessment Study in ACE Intolerant Subjects With Cardiovascular Disease (TRANSCEND) studies.6,7 They estimated 24-hour urinary sodium and potassium excretion from a morning fasting urine sample noting sodium and potassium excretions of 4.77 g and 2.19 g/d, respectively. Compared with the baseline sodium excretion of 4.0 g to 5.99 g of sodium per day, CV death was increased by 9.7% in the group with 7 g to 8 g of sodium excretion per day and by 11.2% in the group with >8 g of sodium per day. There was also an 8.6% increase in CV death and hospitalizations for congestive heart failure in the group with <3 g of sodium excretion per day, indicating a J-shaped curve between sodium excretion and CV events.
Stolarz-Skrzypek and colleagues8 also reported an association of lower sodium excretion and higher CV mortality. In this prospective population study of 3681 participants (who were family members of participants enrolled in the Flemish study on genes, environment, and health outcomes and the European project on genes in hypertension),9,10 2096 participants were normotensive at baseline. CV deaths across tertiles of 24-hour urine sodium excretion were highest (50 of 1220) in the low sodium excretion tertile (mean Na 106 mmol/d) compared with 24 of 1250 in the middle sodium excretion tertile (mean Na 165 mmol/d) and 10 of 1211 in the highest sodium excretion tertile (mean 250 mmol/d; P=.001). Although systolic blood pressure and diastolic blood pressure changes over time aligned with changes in sodium excretion, this association did not translate into higher risk of hypertension and CVD complications from blood pressure.
Reasons proposed for why low sodium could increase CVD include an increase in sympathetic nervous system activation, decreased insulin sensitivity, and activation of the renin-angiotensin-aldosterone-system with progressive sodium restriction.11
What conclusions can we draw from the available data without large-scale prospective studies specifically addressing this question? Our take on the current situation is that the 2300 mg of sodium daily, as recommended by the original American Heart Associations guidelines, represents the best balance of what a hypertensive patient can likely achieve and which is usually within the nadir in these J-curve associations.
To convert sodium to salt, multiply the sodium figure in milligrams (mg) by 2.5 and then divide by 1000.
- 1US Department of Health and Human Services. Dietary Guidelines for Americans 2005, Vol. 6th edn. Washington, DC: US Department of Health and Human Services, US Department of Agriculture; 2005. http://www.health.gov/dietaryguidelines/dga2005/document/pdf/dga2005.pdf. Accessed February 6, 2012.
- 2Institute of Medicine. Strategies to Reduce Sodium Intake in the United States. http://iom.edu/Reports/2010/Strategies-to-Reduce-Sodium-Intake-in-the-United-States.aspx. Accessed February 6, 2012.
- 3Centers for Disease Control and Prevention. Application of lower sodium intake recommendations to adults – United States; 1999–2006. Morb Mortal Wkly Rep. 2009;58:281–283.